Pathophysiology 10

Front 1

Blood Vessels

Back 1

 Arteries—arterioles

 Transport blood away from heart

 Veins—venules

 Return blood back to the heart

 Capillaries

 Microcirculation within tissues

 Systemic circulation

 Exchange of gases, nutrients, and wastes intissues

 Pulmonary circulation

 Gas exchange in lungs

Front 2

Histology of Arteries and Veins

Back 2

Tunica intima—endothelium (simplesquamous epithelium)

Tunica media—middle layer, mostly smoothmuscle

Tunica adventitia (externa)—connectivetissue with fibrocytes, collagen (type I), andelastic fibers

Front 3

Composition of Blood

Back 3

Plasma Plasma proteins Cellular component Erythrocytes Leukocytes Thrombocytes (platelets)

deffence system!

avrg human has 4-5L of blood

pg 186*

Front 4

Erythrocytes

Back 4

(Red Blood Cells) Biconcave flexible discs No nucleus in mature state Contains hemoglobin Globin portion Heme group Life span—120 days Erythropoietin produced in the kidney stimulates erythrocyte production.

Front 5

Hematopoiesis

Back 5

the process of making blood cells

Hematopoiesisstem cell; can become any kind of blood cell

Front 6

Blood Clotting—Hemostasis

Back 6

Three steps:

 Vasoconstriction or vascular spasm after injury

 Platelet clot

 Coagulation mechanism

*Plasmin will eventually break down the bloodclot.

Front 7

Blood Typing

Back 7

Blood typing is based on antigens in the plasmamembrane of the erythrocytes.

 ABO system

 Based on the presence or absence of specificantigens

 Antibodies in the blood plasma

Front 8

Rh system

Back 8

 Antigen D in plasma membrane: Rh+  Absence of antigen D: Rh

Front 9

Diagnostic Tests

< Complete blood count (CBC)

Differential count for WBCs >

Back 9

-Includes total red blood cells (RBCs), white bloodcells (WBCs), and platelets

-Leukocytosis (increased WBCs)

• Associated with inflammation or infection Leukopenia (decreased WBCs)

• Associated with some viral infections, radiation,chemotherapy Increased eosinophils

• Common in allergic responses

-Increased eosinophils

• Common in allergic responses

-Differential count for WBCs

Front 10

Diagnostic Tests :Morphology

Back 10

Observed with blood smears Shows size, shape, uniformity, maturity of cells• Different types of anemia can be distinguished.

Front 11

Diagnostic Tests :Hematocrit

Back 11

Percent by volume of cellular elements in blood

Front 12

Diagnostic Tests:Hemoglobin

Back 12

-Amount of hemoglobin per unit volume of blood

-Mean corpuscular volume (MCV)

• Indicates the oxygen-carrying capacity of blood

Front 13

Diagnostic Tests : Reticulocyte count

Back 13

Assessment of bone marrow function

Front 14

Diagnostic Tests :Chemical analysis

Back 14

Determines serum levels of components, such as iron,vitamin B12, folic acid, cholesterol, urea, glucose

Front 15

Diagnostic Tests : Bleeding time

Back 15

Measures platelet function

Front 16

Diagnostic Tests

< Prothrombin time (PT) and partial thromboplastin time (PTT) >

Back 16

-Measure function of various factors in coagulation process

-International normalized ratio (INR) is a standardizedversion.

Front 17

blood therapies

Whole blood, packed red blood cells, packed platelets

Back 17

For severe anemia or thrombocytopenia

Front 18

blood therapies

Plasma or colloid volume-expanding solutions

Back 18

To maintain blood volume (will increase ossmois)

Front 19

blood therapies

Artificial blood products

Back 19

 Compatible with all blood types

 None of them can perform all the complex functions of normal whole blood.

Front 20

Epoetin alfa

Back 20

-Artificial form of erythropoietin

• Before certain surgical procedures

• Anemia related to cancer

• Chronic renal failure

Front 21

Bone marrow or stem cell transplantation

Back 21

-Close tissue match necessary

• Treatment of some cancers

• Severe immunodeficiency

• Severe blood cell diseases

Front 22

Drug treatment Aids

Back 22

in the clotting process

Front 23

Anemia

Back 23

causes a reduction in oxygen transport. Basic problem is hemoglobin deficit

Front 24

Oxygen deficit leads to:

Back 24

Less energy production in all cells

• Cell metabolism and reproduction diminished Compensation mechanisms

• Tachycardia and peripheral vasoconstriction General signs of anemia

• Fatigue, pallor (pale face), dyspnea, tachycardia

Front 25

Oxygen deficit leads to CONT!

Back 25

Decreased regeneration of epithelial cells

• Digestive tract becomes inflamed and ulcerated, leading to stomatitis

• Inflamed and cracked lips

• Dysphasia

• Hair and skin may show degenerative changes. Severe anemia may lead to angina or congestive heart failure (CHF)

Front 26

Iron Deficiency Anemia

Back 26

-Insufficient iron impairs hemoglobin synthesis. Microcytic, hypochromic RBCs

• Result of low hemoglobin concentration in cells

-Very common

•Ranges from mild to severe

•Occurs in all age groups, but more common in women of childbearing age (d/t menstration)

-Estimated that one in five women is affected

• Proportion increases for pregnant women Frequently sign of an underlying problem

Front 27

Iron Deficiency Anemia: Causes

Back 27

-Dietary intake of iron below minimum requirement

-Chronic blood loss: As from bleeding, ulcer, hemorrhoids, cancer Impaired duodenal absorption of iron In many disorders, malabsorption syndromes

-Severe liver disease May affect iron absorption as well as storage

Front 28

Iron Deficiency Anemia: Signs and Symptoms

Back 28

-Pallor of skin and mucous membranes

-Fatigue, lethargy, cold intolerance

-Irritability - (CNC response * ASK)

-Degenerative changes

-Stomatitis and glossitis

-Menstrual irregularities

-Delayed healing

-Tachycardia, heart palpitations, dyspnea, syncope

Front 29

Pernicious Anemia: Vitamin B12 Deficiency

Back 29

Basic problem is lack of absorption of vitamin B12 because of lack of intrinsic factor

~ Intrinsic factor secreted by gastric mucosa

~ Required for intestinal absorption of vitamin B12

Characterized by very large, immature, nucleated erythrocytes

Carry less hemoglobin Shorter life span ( reg is 120 days)

Front 30

Pernicious Anemia: Vitamin B12 Deficiency (Cont.)

Back 30

 Dietary insufficiency is very rarely a cause.

Genetic factors have been implicated.

~More common in light-skinned women of northern European ancestry

 Often accompanies chronic gastritis

 May also be an outcome of gastric surgery

Front 31

Vitamin B12 and Nerve Cells

Back 31

-Vitamin B12 is needed for the function and maintenance of neurons.

-Significant deficit of the vitamin will cause symptoms in the peripheral nerves.

-These may be reversible.

Front 32

Pernicious Anemia: Vitamin B12 Deficiency (Cont.) Manifestations in addition to those typical for anemias + plus

Back 32

 Tongue is typically enlarged, red, sore, and shiny.

 Digestive discomfort, often with nausea and diarrhea

 Feeling of pins and needles, tingling in limbs

Front 33

Diagnostic tests for pernicious anemia

Back 33

-Microscopic examination (erythrocytes)

-Bone marrow examination (hyperactive)

-Vitamin B12 serum levels below normal

-Presence of hypochlorhydria or achlorhydria

•Presence of gastric atrophy

Front 34

Aplastic Anemia

Back 34

Impairment or failure of bone marrow

-May be temporary or permanent

-Often idiopathic but possible causes include: Myelotoxins

• Radiation, industrial chemicals, drugs

Viruses

• Particularly hepatitis C

Genetic abnormalities

• Myelodysplastic syndrome

• Fanconi’s anemia Blood counts indicate pancytopenia.

Anemia, leukopenia, thrombocytopenia Bone marrow biopsy may be required. Erythrocytes often appear normal. Identification of cause and prompt treatment needed for bone marrow recovery Removal of any bone marrow suppressants Failure to identify cause and treat effectively is life-threatening!

Front 35

Hemolytic Anemia

Back 35

 Results from excessive destruction of RBCs

 Causes

 Genetic defects

 Immune reactions

 Changes in blood chemistry

 Infections such as malaria

 Toxins in the blood

 Antigen-antibody reactions • Incompatible blood trans

*CBC's, hematocrit, hemoglobin: would be lower.

Front 36

Sickle Cell Anemia

Back 36

Genetic condition Autosomal Incomplete dominance Anemia occurs in homozygous recessive. Diagnostic testing is available. More common in individuals of African ancestry• Heterozygous condition is somewhat protective againstmalaria.• One in ten African Americans is heterozygous for thetrait.

Front 37

Sickle Cell Anemia (Cont.)

Back 37

Abnormal hemoglobin (HbS) Sickle cell crisis occurs whenever oxygenlevels are lowered. Altered hemoglobin is unstable and changesshape in hypoxemia. Sickle-shaped cells are too large to passthrough the microcirculation. Obstruction leads to multiple infarctions andareas of necrosis.

Front 38

Sickle Cell Anemia (Cont.)

Back 38

Multiple infarctions affect brain, bones,organs In addition to basic anemia: Hyperbilirubinemia, jaundice, gallstones• Caused by high rate of hemolysis Clinical signs Do not usually appear until the child is about 12months old

Front 39

Sickle Cell Anemia: Signs and Symptoms

Back 39

Severe pain because of ischemia of tissues andinfarction Pallor, weakness, tachycardia, dyspnea Hyperbilirubinemia—jaundice Splenomegaly Vascular occlusions and infarctions In lungs• Acute chest syndrome Smaller blood vessels• Hand-foot syndrome Delay of growth and development Congestive heart failure

Front 40

Sickle Cell Anemia - Diagnostic tests

Back 40

 Blood test• Hemoglobin electrophoresis Prenatal DNA analysis

Front 41

Sickle Cell Anemia - Treatment

Back 41

 Hydroxyurea has reduced the frequency of this crisis.  Dietary supplementation with folic acid  Bone marrow transplantation  Immunization in children • Against pneumonia, influenza, meningitis

Front 42

Polycythemia

Back 42

Primary polycythemia—polycythemia vera

- Increased production of erythrocytes and othercells in the bone marrow

- Neoplastic disorder

- Serum erythropoietin levels are low.

Secondary polycythemia—erythrocytosis

- Increase in RBCs in response to prolongedhypoxia

- Increased erythropoietin secretion

- Compensation mechanism to provide increasedoxygen transport

Front 43

Polycythemia: Signs and Symptoms

Back 43

Distended blood vessels, sluggish blood flow

Increased blood pressure

Hypertrophied heart (inlarged)

Hepatomegaly Splenomegaly

Dyspnea Headaches

Visual disturbances Thromboses and infarctions

Front 44

Polycythemia - Diagnostic tests

Back 44

Increased cell counts

Increased hemoglobin and hematocrit values Hypercellular bone marrow

Hyperuricemia (higher acid in urine)

Front 45

Polycythemia - Treatment

Back 45

 Identify cause

 Drugs or radiation

• Suppression of bone marrow activity

 Periodic phlebotomy (taking lots of blood)

Front 46

Indications of Blood-Clotting Disorders

***measuments**

Back 46

Persistent bleeding from gums

Repeated epistaxis

Petechiae - Pinpoint, flat, red spots on skin and mucousmembrane

Frequent purpura and ecchymosis

More than normal bleeding in trauma

Bleeding into joint—hemarthroses Swollen, red, painful Hemoptysis

Front 47

Blood-Clotting Disorders

Back 47

 Hematemesis - Coarse brown particles (coffee ground emesis)

 Blood in feces - Black or occult

 Anemia

 Feeling faint and anxious

 Low blood pressure Rapid pulse

Front 48

Hemophilia A

Back 48

 Classic hemophilia - Deficit or abnormality of factor VIII

 Most common inherited clotting disorder

- X-linked recessive trait

- Manifested in men, carried by women

 Varying degrees of severity

 Prolonged bleeding after minor tissue trauma

 Spontaneous bleeding into joints

 Possible hematuria or blood in feces

Front 49

Hemophilia A - Diagnostic tests

Back 49

 Bleeding time and PT normal

 PTT, activated PTT (aPTT), coagulation timeprolonged

 Serum levels of factor VIII are low.

Front 50

Hemophilia A - Treatment

Back 50

 Desmopressin (DDAVP)

 Replacement therapy for factor VIII

Front 51

Von Willebrand’s Disease

Back 51

 Most common hereditary clotting disorder

 Three major types

Front 52

Von Willebrands Disease - Signs and symptoms include:

Back 52

 Skin rashes  Frequent nosebleeds  Easy bruising  Bleeding of gums  Abnormal menstrual bleeding

 Treatment based on type and severity

Front 53

Disseminated Intravascular Coagulation

Back 53

Involves both excessive bleeding and clotting Excessive clotting in circulation Thrombi and infarcts occur. Clotting factors are reduced to a dangerous level. Widespread, uncontrollable hemorrhage results. Very poor prognosis, with high fatality rate Complication of many primary problems Obstetrical complications, such as abruptio placentae Infections Carcinomas Major trauma

Front 54

Thrombophilia

Back 54

Group of inherited or acquired disorders Risk of abnormal clots in veins or arteries Blood testing for clotting factor levels andabnormal antibody levels Causative condition should be treated.

Front 55

Myelodysplastic Syndromes

Back 55

Diseases that involve inadequate productionof cells by the bone marrow

Signs and symptoms include anemia;dependent on type of deficiencies that occur

May be idiopathic or occur afterchemotherapy or radiation treatment

Treatment measures depend on deficiencytype.

- Transfusion replacement

- Chelation therapy to reduce iron overload

- Bone marrow transplantation

Front 56

The Leukemias

Back 56

Group of neoplastic disorders involving white bloodcells Uncontrolled WBC production in bone or lymphnodes Other hemopoietic tissues are reduced. One or more types of leukocytes are undifferentiated,immature, and nonfunctional. Large numbers released into general circulation Infiltrate lymph nodes, spleen, liver, brain, otherorgans

Front 57

Acute leukemias (ALL and AML)

Back 57

- High proportion of immature nonfunctional cells inbone marrow and peripheral circulatio

- Onset usually abrupt , marked signs ofcomplications• Occurs primarily in children and younger adults

Front 58

Chronic leukemias (CLL and CML)

Back 58

 Higher proportion of mature cells

 Insidious onset

 Mild signs and better prognosis • Common in older adults

Front 59

Signs and Symptoms of Acute Leukemia

Back 59

Usual signs at onset

-Frequent or uncontrolled infections

-Petechiae and purpura

-Signs of anemia

~Severe and steady bone pain

~Weight loss, fatigue, possible fever

~Enlarged lymph nodes, spleen, liver

~Headache, visual disturbances, drowsiness,vomiting

Front 60

The Leukemias - Diagnostic tests

Back 60

Peripheral blood smears• Immature leukocytes and altered numbers of WBCs• Numbers of RBCs and platelets decreased• Bone marrow biopsy for confirmation

Front 61

The Leukemias - Treatment

Back 61

Chemotherapy ALL in young children responds well to drugs Biological therapy (interferon)• May be used to stimulate the immune system

Front 62

Complications of Leukemia

Back 62

-Opportunistic infections, including pneumonia

-Sepsis

-Congestive heart failure

-Hemorrhage

-Liver failure

-Renal failure

-CNS depression and coma

Front 63

Multiple Myeloma

Back 63

-Neoplastic disease that involves increasedproduction of plasma cells in bone marrow

-Unknown cause

-Occurs in older adults

-Production of other blood cells is impaired

-Multiple tumors in bone

-Loss of bone

-Severe bone pain

-Prognosis poor, with short life expectancy